ライフサイエンスコーパス: cyclooxygenase inhibitor

1 SC 58125, a newly developed PGHS-2-selective cyclooxygenase inhibitor.

2 aglandin synthesis in wild-type mice using a cyclooxygenase inhibitor.

3 tantially reduced by treating B6 mice with a cyclooxygenase inhibitor.

4 ision of any of three structurally different cyclooxygenase inhibitors.

5 yl methylation of gamma subunits elicited by cyclooxygenase inhibitors.

6 and the 5-LO inhibitor zileuton, but not by cyclooxygenase inhibitors.

7 S-induced IPCs from the SGZ is suppressed by cyclooxygenase inhibitors.

8 ed small intestinal ulcers despite no use of cyclooxygenase inhibitors.

9 origenic and chemopreventive drugs including cyclooxygenase inhibitors.

10 ely control zinc stores by their activity as cyclooxygenase inhibitors.

11 a narrow singlet in complexes of PGHS-2 with cyclooxygenase inhibitors.

12 T was rescued both in vitro and in vivo with cyclooxygenase inhibitors.

13 by lipoxygenase, but not cytochrome P450 or cyclooxygenase inhibitors.

14 thdrawal due to adverse events compared with cyclooxygenase inhibitors.

15 landins, prostaglandin receptor agonists, or cyclooxygenase inhibitors.

16 , 6-dihydro-15-F2t-IsoP were not affected by cyclooxygenase inhibitors.

17 Cyclooxygenase inhibitors abrogated the response of earl

18 nflammatory compound indomethacin, a general cyclooxygenase inhibitor, affected obesity development a

19 Cyclooxygenase inhibitors also reduced the tumor phenoty

20 be activated by indomethacin, a nonselective cyclooxygenase inhibitor and widely used nonsteroidal an

21 a difference in pain reduction compared with cyclooxygenase inhibitors and glucocorticoids for treati

22 responses evoked by PARs were insensitive to cyclooxygenase inhibitors and were suppressed by agents

23 whereas indomethacin (INDO, 10(-5) mol/L; a cyclooxygenase inhibitor) and N omega-nitro-L-arginine m

24 response was not affected by indomethacin (a cyclooxygenase inhibitor) and sulfaphenazole (an epoxyge

25 ly, angiotensin-converting enzyme inhibitor, cyclooxygenase inhibitor, and dopamine agent, were selec

26 However, indomethacin is not a specific cyclooxygenase inhibitor, and its other pharmacologic ef

27 in or saline; six also received ibuprofen, a cyclooxygenase inhibitor, and six received placebo.

28 Six were randomized to receive ibuprofen, a cyclooxygenase inhibitor, and six were given placebo.

29 Although steroids and cyclooxygenase inhibitors are effective antiinflammatory

30 nderlying the anti-tumorigenic properties of cyclooxygenase inhibitors are not well understood.

31 ith either a COX-1 selective or nonselective cyclooxygenase inhibitor as compared with a COX-2 select

32 Aspirin and indomethacin, both cyclooxygenase inhibitors as well as direct ROS scavenge

33 fen, ibuprofen, diclofenac, ketorolac, etc., cyclooxygenase inhibitors) as agents for the management

34 The cyclooxygenase inhibitor aspirin and the 5-lipoxygenase

35 Suppression of PGE(2) synthesis by the cyclooxygenase inhibitors aspirin and celecoxib suppress

36 spore germination and mycelial growth by two cyclooxygenase inhibitors (aspirin and indomethacin) als

37 ases in cAMP were blocked by indomethacin, a cyclooxygenase inhibitor, (b) arachidonic acid increased

38 In vivo, administration of a cyclooxygenase inhibitor before LPS injection resulted i

39 e functions (cyclooxygenase, peroxidase, and cyclooxygenase inhibitor binding activities) began at Gd

40 ated that 5-lipoxygenase inhibitors, but not cyclooxygenase inhibitors, block IL-1 beta-induced VCAM-

41 Indomethacin, a cyclooxygenase inhibitor, blunted such NBT reduction (1+

42 ed PKA activity by either corticosteroids or cyclooxygenase inhibitors converts the cytokines from in

43 nstream therapies such as corticosteroids or cyclooxygenase inhibitors could fail to address or exace

44 Indomethacin, a cyclooxygenase inhibitor, countered the ICC-SC-mediated

45 pound 1 also showed clear superiority to the cyclooxygenase inhibitors diclofenac and rofecoxib.

46 K(Ca) channel blocker, charybdotoxin, or the cyclooxygenase inhibitor, diclofenac.

47 Cyclooxygenase inhibitors did not abolish 8-iso-PGE(2) m

48 he PGHS substrate, arachidonate, and various cyclooxygenase inhibitors do not alter this binding affi

49 Treatment with cyclooxygenase inhibitors dramatically reduced the viabi

50 The mechanisms by which cyclooxygenase inhibitors exert antitumor effects are no

51 tic benefits of combining 5-lipoxygenase and cyclooxygenase inhibitors for maximal pain inhibition.

52 1 cooperativity is that the affinity of many cyclooxygenase inhibitors for PGHS1 decreases in paralle

53 NSAIDs) associated with better outcomes than cyclooxygenase inhibitors, glucocorticoids, IL-1 inhibit

54 inhibitor) or indomethacin (a non-selective cyclooxygenase inhibitor) had significant reductions in

55 Indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expre

56 In addition, cyclooxygenase inhibitors have been shown to have antine

57 other nonsteroidal antiinflammatory drugs or cyclooxygenase inhibitors have the greatest potential ef

58 oglia were stimulated in the presence of the cyclooxygenase inhibitor ibuprofen, and microglial condi

59 s effect was reversed by the addition of the cyclooxygenase inhibitor, ibuprofen, or a DP1 receptor a

60 Coadministration of the cyclooxygenase inhibitor, ibuprofen, with the TRPV1 anta

61 incubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid

62 w potential applications of these identified cyclooxygenase inhibitors in preventing inflammatory dis

63 l(-1)) or the combination of l-NAME and the cyclooxygenase inhibitor indomethacin (10(-5) mol l(-1))

64 LA2 inhibitor mepacrine (100 microM) and the cyclooxygenase inhibitor indomethacin (2 microM).

65 o-L-arginine methyl ester (20 mg/kg) and the cyclooxygenase inhibitor indomethacin (5 mg/kg).

66 ) phenylephrine, after pretreatment with the cyclooxygenase inhibitor indomethacin (5.0 mg/kg), 10(-4

67 micromol/min intra-arterially), and (3) the cyclooxygenase inhibitor indomethacin (50 mg PO TID).

68 The cyclooxygenase inhibitor indomethacin completely inhibit

69 infected cPLA2alpha+/+ macrophages with the cyclooxygenase inhibitor indomethacin increases TNFalpha

70 , and combined administration of l-NAME with cyclooxygenase inhibitor indomethacin mimicked the effec

71 vity of both porins was not inhibited by the cyclooxygenase inhibitor indomethacin or by neutralizing

72 Treatment with the cyclooxygenase inhibitor indomethacin reduces beta-caten

73 ase in cAMP was prevented by addition of the cyclooxygenase inhibitor indomethacin, consistent with r

74 ting protein inhibitor MK-886 but not by the cyclooxygenase inhibitor indomethacin.

75 ynthase inhibitor alone or combined with the cyclooxygenase inhibitor indomethacin.

76 osis was stimulated by pretreatment with the cyclooxygenase inhibitor indomethacin.

77 Pretreatment with the cyclooxygenase inhibitors indomethacin and flurbiprofen

78 action, which was partially inhibited by the cyclooxygenase inhibitors indomethacin and flurbiprofen.

79 nase C and A inhibitors, H-7 and H-8, or the cyclooxygenase inhibitor, indomethacin, had no effect up

80 The increased transport was blocked by the cyclooxygenase inhibitor, indomethacin, or the specific

81 protein-directed inhibitor MK886 but not the cyclooxygenase inhibitor, indomethacin, reduced growth,

82 bitor, (R)-bromoenol lactone, but not by the cyclooxygenase inhibitor, indomethacin.

83 e epoxygenase inhibitor, miconazole, and the cyclooxygenase inhibitor, indomethacin.

84 , the authors tested whether indomethacin, a cyclooxygenase inhibitor, influences the stimulation of

85 Additionally, the cyclooxygenase inhibitor ketorolac (10 microM) significa

86 -arginine (l-NMMA, 10 mm), the non-selective cyclooxygenase inhibitor ketorolac tromethamine (Keto, 1

87 site structure was probed by examination of cyclooxygenase inhibitor kinetics.

88 Selective cyclooxygenase inhibitors may retard the progression of

89 s, including 13'-carboxychromanol, are novel cyclooxygenase inhibitors, may serve as anti-inflammatio

90 on and the eosinophilia at 24 h, whereas the cyclooxygenase inhibitor, meclofenamic acid (5 mg/kg, in

91 re and after incubation with indomethacin (a cyclooxygenase inhibitor), N(G)-nitro-L-arginine (an NO

92 Bay y 1015 and Bay x 1005, and the cyclooxygenase inhibitor naproxen, were evaluated indivi

93 Similarly, the cyclooxygenase inhibitor, naproxen, had no effect on the

94 e prevented by peripheral treatment with the cyclooxygenase inhibitor nimesulide or the aromatase inh

95 Addition of a cyclooxygenase inhibitor, nimesulide, similarly resulted

96 Cyclooxygenase inhibitors, nitric oxide synthase inhibit

97 Neither sulindac sulfide (a cyclooxygenase inhibitor) nor sulindac sulfone induced G

98 The cyclooxygenase inhibitors, NS-398 and indomethacin, were

99 of this study was to examine the effects of cyclooxygenase inhibitors on basic fibroblast growth fac

100 In contrast, the effects of cyclooxygenase inhibitors on the stability of the prefor

101 ction, we analyzed the effects of PGE(2) and cyclooxygenase inhibitors on this process.

102 ced in diabetic rats by spinal delivery of a cyclooxygenase inhibitor or an EP(1) receptor antagonist

103 sured after intrathecal delivery of either a cyclooxygenase inhibitor or an EP(1) receptor antagonist

104 We speculate that the binding of cyclooxygenase inhibitors or AA to the cyclooxygenase si

105 tored (10-30%) by treating H386A PGHS-1 with cyclooxygenase inhibitors or AA, but not with linoleic a

106 ivity was reversible and was not mimicked by cyclooxygenase inhibitors or by cycloheximide.

107 ia with prior administration of ibuprofen, a cyclooxygenase inhibitor, or dimeric p75 tumor necrosis

108 ment with either indomethacin (5 mumol/L), a cyclooxygenase inhibitor, or NG-nitro-L-arginine methyl

109 that was sensitive to either indomethacin, a cyclooxygenase inhibitor, or SQ29548, a selective thromb

110 At 120 mins of endotoxemia, indomethacin (cyclooxygenase inhibitor) plus L-NAME markedly increased

111 ating protein-directed inhibitors, but not a cyclooxygenase inhibitor, reduced growth, increased apop

112 Cyclooxygenase inhibitors represented extremely promisin

113 he discrepancy between the concentrations of cyclooxygenase inhibitors required to produce anti-neopl

114 to a wide singlet species; pretreatment with cyclooxygenase inhibitors results in a third type of sig

115 AR reporter gene activation was induced in a cyclooxygenase inhibitor-sensitive manner, an effect tha

116 High doses of cyclooxygenase inhibitors substantially block viral repl

117 nonsteroidal anti-inflammatory drug (NSAID) cyclooxygenase inhibitors such as ibuprofen, naproxen, a

118 The structure of this radical is altered by cyclooxygenase inhibitors, such as indomethacin and flur

119 ple topical administration of a non-specific cyclooxygenase inhibitor, suggesting the involvement of

120 when cells were treated with indomethacin, a cyclooxygenase inhibitor that blocks the synthesis of PG

121 steroidal anti-inflammatory drug (NSAID) and cyclooxygenase inhibitor that is frequently used as a re

122 nchoconstriction in response to nonselective cyclooxygenase inhibitors that deplete homeostatic PGE2.

123 e therapies, the risks of relapse from using cyclooxygenase inhibitors, the lack of benefit from lipo

124 When cyclooxygenase inhibitors were added with the AA, the an

125 decoxib) from the diarylheterocycle class of cyclooxygenase inhibitors were radiolabeled and used to

126 ibition by D- and L-ibuprofen, a competitive cyclooxygenase inhibitor, were 32, 67, and 7.1 for nativ

127 an serum albumin (HSA-III) and diflunisal, a cyclooxygenase inhibitor with antiinflammatory activity.

128 pothesized that indomethacin, a nonselective cyclooxygenase inhibitor, would diminish allergen-induce